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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_2853_Библиотеки_им_академика_М_И_Перельмана
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Talc deposits. White or yellow spots in the retinas of intravenous drug users
result from injecting ground-up tablets containing talc.
Cytomegalovirus (CMV) retinitis.
infection is accompanied by cytomegalovirus infection of the retina.
describe visual loss, blurring, oaters, and ashes of light. Look for whitening of the retina, cotton-wool spots, and intraretinal hemorrhages. Although
less common, consider varicella zoster infection, toxoplasmosis, and syphilis.
CMV retinitis is uncommon with the advent of highly active antiviral therapy.
Candida endophthalmitis. Systemic Candida infection associated with
immunosuppression and indwelling venous catheters is difcult to diagnose.
Patients have fever, but blood cultures are often negative. Small white patches
on the retina may be the only sign of disease. With advancing disease, there is
pain, visual disturbance, and large white globular lesions invade the vitreous.
Macular degeneration. Vision is much reduced, but the only visible sign may
be a few spots of pigment near the macula and blurring of the macular borders. In other cases, subretinal hemorrhages, patches of atrophy, yellow drusen, and pigmented areas are seen.
Retinitis pigmentosa. Inherited singly or as a component of several syndromes, retinitis pigmentosa manifests arteriolar narrowing, waxy pallor
of the optic disc, and perivascular retinal pigmentation. Night blindness is
the earliest symptom, but all types of vision become impaired as the retina
degenerates progressively from the periphery to the posterior retina. Spidery
strands of pigmented spots form a girdle about the global equator (Fig. 7-53A).
Angioid streaks. Probably the result of elastic tissue degeneration, broad
lines of pigment radiate from the optic disk, branching like blood vessels (Fig. 7-53B). They occur in Paget disease and in pseudoxanthoma
elasticum.
Advanced immunosuppression from HIV
Patients
FIG. 7-53 Retinal Pigmentation.
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FIG. 7-54 Retinal Detachment.
Retinal detachment. Retinal detachments are symptomatic or asymptomatic.
Patients complain of ashing lights followed by oaters and then a curtain
crossing their vision. The earliest sign is elevation of an area of retina placing
it out of focus with surrounding structures. The arteries and veins in the separated membrane appear elevated (Fig. 7-54). When markedly detached, the
retina becomes a folded gray sheet. Underlying inammation produces areas
of choroiditis and vitreous opacities. The edge of a tear is horseshoe shaped.
The cause of detachment is often undetermined.
Nose and Sinus Signs
Epistaxis (nosebleed). The most common bleeding site is Kiesselbach plexus,
a vascular network on the anterior nasal septum. Posterior hemorrhage frequently occurs at the back third of the inferior meatus from large vessels supplied by the external carotid artery. In some cases, there are multiple oozing
points in the mucosa. A Nosebleed can be spontaneous and trivial or a sign
of serious local or generalized disease. Hemorrhage from the external nares
is obvious, but bleeding from the choana needs to be distinguished from
hemoptysis and hematemesis. In approaching epistaxis, the rst challenges
are to identify the bleeding site and determine whether trauma or a predisposing condition is present. Observe universal precautions with gloves,
gown, and face protection. Remove clots by suction or by having the patient
clear the nose by blowing. Inspect the anterior nasal chambers, especially
the septum. If profuse hemorrhage obscures the site, advance the suction tip
backward in small increments until the point where the passage immediately
lls after clearing; this is the bleeding site. Blood-tinged uid suggests a CSF
leak. Consult textbooks for methods of arresting hemorrhage.
CLINICAL OCCURRENCE: Local Causes: Coughing, sneezing, nose pick-
ing, fractures, lacerations, foreign bodies, adenoid growth, nasopharyngeal
broma, angioma, rhinitis sicca.
Generalized Causes: Congenital: Hereditary
hemorrhagic telangiectasia; Infectious: Viral rhinitis, typhoid fever, scarlet
fever, inuenza, measles, infectious mononucleosis, diphtheria, pertussis,
psittacosis, Rocky Mountain spotted fever, erysipelas, mucosal leishmaniasis; Inammatory/Immune: Granulomatosis with polyangiitis (Wegener),
lethal midline granuloma; Mechanical/Traumatic: (see local causes) Changes in
atmospheric pressure (mountain climbing, caisson disease, ying) exertion;
Metabolic/Toxic: Pernicious anemia, aspirin, scurvy; Neoplastic: Nasopharyngeal
carcinoma, squamous cell carcinomas, leukemia; Vascular: Coagulopathy,
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cirrhosis, uremia, hemophilia, von Willebrand disease, thrombocytopenia,
hypertension, aortic coarctation; Elevated venous pressure: Cor pulmonale, congestive heart failure, superior vena cava syndrome.
Nasal and maxilla fracture. Nasal fractures are simple or comminuted;
seldom are they compound. A blow from the side displaces both nasal
bones to the opposite side, producing an S-shaped curve in the dorsum
nasi. The septum is fractured with or without nasal bone fracture. Frontal
blows depress the nasal bones. If palpation along the inferior border of
the orbit discloses an irregularity, maxilla fracture is present; a fragment
may displace downward into the sinus. Malocclusion of the teeth indicates
displacement of the maxilla. Fracture of the zygoma produces attening of
the cheek.
Anosmia.
nerve endings passing through the cribriform plate, produce loss of smell.
Anosmia is invariably accompanied by a perceived change in taste with food
seeming bland and unpalatable. The most common identied cause is closed
head trauma. This can be an early sign of Parkinson diseases or Alzheimer
dementia.
Congenital nasal deformities. Disturbances in nasal development are myriad. The most common is cleft nose from incomplete fusion at the tip and
dorsum (Fig. 7-55B).
Acquired nose deformities. Acquired deformities are the result of trauma,
infection, or neoplasms. Rhinophyma is an erythematous bulbous enlargement of the distal two-thirds of the nose from multiple sebaceous adenomas
(Fig. 7-55A). It may follow long-standing rosacea. Saddle nose has a sunken
bridge (Fig. 7-55C) resulting from loss of cartilage; common causes are septal
hematoma or abscess. Rarely, it is caused by relapsing polychondritis, granulomatosis and polyangiitis (Wegener), or congenital or acquired syphilis. A
crooked nose results from fracture.
Vestibule folliculitis. Mild inammation around the hair follicles is evident
on inspection.
Vestibule furunculosis. A small supercial abscess forms in the skin or
mucous membrane. The area is extremely tender, swollen, and reddened.
Nasal obstruction and CN-I injury, often by traumatic shearing of
FIG. 7-55 External Nasal Deformities. A. Rhinophyma. B. Cleft nose. C. Saddle nose: Note the sinking of
the dorsum with relative prominence of the lower third.
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FIG. 7-56 Lesions in the Nasal Vestibule. A. Furuncle: Avoid trauma that might spread infection to the cavernous
sinus. B. Perforation of nasal septum: Transillumination of the septum discloses a hole.
Swelling may involve the nasal tip, alae nasi, and upper lip (Fig. 7-56A).
Avoid instrumentation or other trauma to pyogenic lesions within the triangle anterior to a line from the corners of the mouth to the glabella as it may
spread infection directly to the cavernous sinus.
Fissure. Fissures developing at the mucocutaneous junction become overlaid
with crusts covering the tender surfaces.
Deviated septum. The nasal septum is seldom precisely a midline structure.
The cartilaginous and bony septum may deviate as a hump, spur, or shelf
encroaching on one chamber, occasionally causing obstruction.
Perforated septum. The cartilaginous septal perforation is caused by chronic
infection, repeated trauma in picking off crusts, nasal or transphenoidal pituitary surgery, or cocaine abuse. Perforation is discovered by looking in one
naris while shining a light in the other (Fig. 7-56B).
Septum hematoma. Even slight nasal trauma produces bleeding under the
mucoperichondrium, often causing bilateral hematomas. Nasal obstruction
necessitates breathing through the mouth. The hematoma is a violaceous,
compressible, obstructive mass. The columella may be widened and the nasal
tip pales from stretching of the skin. Pressure from the hematoma on the anterior ethmoidal nerve may cause anesthesia of the tip. Hematomas may compromise the septum’s blood supply resulting in slow cartilage necrosis and
saddle nose deformity.
Septal abscess. The edematous septum swells into both nasal chambers.
Infected septal hematomas invariably result in loss of cartilage. Immediate
incision and drainage plus appropriate antibiotics lowers risk for progression
through the angular veins to produce cavernous sinus thrombosis.
Foreign body. Children frequently put objects into the nose that, remaining
for extended periods, produce foul, purulent unilateral discharge.
Neoplasm. Sinus carcinomas cause obstruction, bloodstained discharge,
constant boring pain, and they invade bone. Invasion of the orbit causes
ocular disturbances, of the maxillary antral oor loosening upper teeth
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and/or leading to an ill-tting denture. The hard palate may bulge and
become soft.
Cerebrospinal uid (CSF) rhinorrhea.
the subarachnoid space and nasal cavity.
unilateral discharge of clear spinal uid develops. The uid may be blood
tinged but is easily distinguished from a nosebleed. Jugular vein compression increases the ow. If spinal uid is suspected, test a specimen for
beta-2-transferrin. Substantial risk for meningitis and recurrent meningitis
demands a search for CSF leak.
Nasal discharge—acute suppurative sinusitis. See page 248.
Nasal discharge—chronic suppurative sinusitis. See page 249.
Sinusitis and periorbital edema—periorbital abscess. See page 241.
Sinusitis and periorbital edema—orbital cellulitis. See page 241.
Sinusitis and ocular palsies—cavernous sinus thrombosis. See page 249 and
Figure 7-57A.
Nasal polyps.
developing after recurrent episodes of mucosal edema. They are frequently
seen in long-standing allergic rhinitis, aspirin-sensitive asthma, and cystic
brosis. Polyps are commonly multiple, most frequently protruding from the
middle meatus as smooth, pale, spheric mucosal masses (Fig. 7-57B). Polyps
may enlarge obstructing the air passages; they frequently recur after removal.
DDX: Polyps are mobile and insensitive, distinguishing them from swollen
turbinates.
Periorbital masses—mucocele and pyocele.
frontal or ethmoid sinus orifices causes mucus secreted by their mucosae
to accumulate. The resulting sac, or mucocele, slowly enlarges, the pentup mucus exerts pressure on surrounding structures and erodes bone,
behaving like a neoplasm. The sac may eventually erode into the frontal
sinus or lateral ethmoid wall producing painless swelling beneath the
supraorbital ridge, medial to the globe (Fig. 7-58).
rubbery and slightly compressible. The globe is pushed downward and
laterally, causing diplopia; proptosis may also occur. Upward and medial
eye motions are restricted. Intranasal examination may be negative. An
infected mucocele is a pyocele. DDX: Swelling from a mucocele is above
the inner canthus; dacryocystitis causes swelling below the canthus.
Nasal polyps are sessile or pedunculated mucosal overgrowths
A traumatic stula is created between
After head injury or surgery, a
Permanent obstruction of the
The painless mass feels
Papillomas. Benign papillomas, often in the vestibule, are slow-growing sinus
neoplasms, usually osteomas or chondromas. They are asymptomatic until air
passages or a sinus orice is obstructed. Inverted papillomas grow downward
into the underlying tissues so are difcult to resect.
Granulomatosis and polyangiitis (Wegener). See Chapter 8, page 362.
A. Cavernous sinus thrombosis B. Nasal polyps
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FIG. 7-57 Lesions About the Nose. A. Cavernous sinus thrombosis: Early there is paralysis of a single ocular
muscle, with the development of edema and proptosis (shown). B. Nasal polyps: The parasagitt al section shows the lateral
wall with three polyps emerging from the middle meatus.
a
Internal angular
d
duct
l
dermoid
lacrimal gland
frontal sinus
FIG. 7-58 Some Masses About the Orbit. A. Mucocele of frontal sinus: An example of a mucocele, this occur-
ring in the floor of the supraorbital ridge and presenting medially. B. Locations of masses about the eye.
orbital swellings
Breath Signs
Breath odor. There is great variation in olfactory acuteness, and description of
odors is meaningless; experience is necessary. A foul breath odor, fetor oris, is
common in infection (dental, tonsillar), atrophic rhinitis, putrefaction of food
(achalasia, esophageal diverticula, pyloric obstruction), and infected sputum
(bronchiectasis, lung abscess). Acetone on the breath indicates ketonemia in
diabetic or starvation acidosis. In some uremic patients, ammonia is detected.
A curious musty odor occasionally is smelled with severe liver disease. Inhalation or ingestion of volatile hydrocarbons produces detectable odor in exhaled
air. Alcohol on the breath indicates recent ingestion, but medical illness,
trauma, or ingestion of other drugs must be excluded as comorbid conditions. A few comatose patients don’t have alcohol breath odor, but aspirated
gastric contents smell strongly of alcohol. The chronic alcoholic may smell of
acetaldehyde instead of alcohol. The methyl mercaptan causing garlic’s odor is
excreted from the lungs for >24 hours.
Lip Signs
Cleft lip. Incomplete fusion of the frontonasal process with the two maxillary
processes leaves a persistent cleft in one or both sides of the upper lip, sometimes accompanied by cleft palate.
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Lip enlargement. The lips may appear large in cretinism, myxedema, acromegaly, and collagen injections.
Lip vesicles—herpes simplex (cold sores, fever blisters).
herpes simplex virus induces local inammation, often when the carrier
develops another infectious disease, has local trauma, or is exposed to sunlight.
Groups of vesicles containing clear uid are surrounded by areas of
erythema, frequently on the lips. The lesions burn or smart.
Cheilosis (angular stomatitis). Maculopapular and vesicular lesions
are grouped at the corners of the mouth and the mucocutaneous junction
(Fig. 7-59A). Skin irritation leads to crusting and ssuring. Often accompanying profuse salivation from any cause, it is specically associated with
riboavin deciency and ill-tting dentures. Secondary Candida infection is
common (perlèche). The entire lip becomes inamed from overexposure to
sunlight, actinic cheilosis.
Carbuncle. Painful localized swelling with erythema and increased skin
warmth suggests early cellulitis or carbuncle. On the upper lip, it is exceedingly dangerous, the veins draining into the cavernous sinus.
Lip carcinoma. Early lesions are indurated and discoid, later, becoming
warty and crusted, forming a slowly extending shallow ulcer. The ulcerated
border is elevated, sometimes pearly (Fig. 7-59B). Regional lymph nodes are
involved late. It is more frequent in men and 95% are on the lower lip. Biopsy
all the ulcers >2 weeks old.
Lip chancre. The initial lesion of syphilis occurs at the inoculation site. The
lip is the most common extragenital site of primary syphilitic chancre; usually
the upper lip is involved. The lesion is discoid, without sharply dened borders and can be moved over the underlying tissues. It soon ulcerates to exude
a clear uid teeming with Treponema pallidum. The regional lymph nodes are
involved early and feel larger and softer than carcinomatous nodes. Serologic
tests for syphilis are frequently negative while the chancre is present.
Reactivating latent
FIG. 7-59 Some Lip Lesions. A. Cheilosis. B. Epidermoid carcinoma of lip: notice the sharply demarcated
elevated edges with the ulcerating base, typically located at the mucocutaneous junction. C. Rhagades. D. Signs of
Peutz–Jeghers syndrome.
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Molluscum contagiosum. A nodular growth in the lip may ulcerate to discharge caseous material. The ulcer border may be elevated. The lesion is
caused by Molluscipoxvirus. The resemblance to carcinoma may be striking,
so biopsy may be required.
Rhagades. The white radial scars about the angles of the mouth are stigmata
of previous syphilitic lesions (Fig. 7-59C).
Actinic keratosis. A dry, at, light-colored precancerous growth occurs on the
lip producing scaling; it bleeds easily.
Lip pigmentation—Peutz–Jeghers syndrome. Multiple pigmented brown to
black spots on the lips resemble freckles (Fig. 7-59D), but freckles are uncommon on the mucosa. This autosomal dominant syndrome is associated with
intestinal polyposis and increased risk for gastrointestinal cancer.
Lip telangiectasias—hereditary hemorrhagic telangiectasia. The most obvious lesions occur on the buccal mucosa, tongue, and lips. See page 153.
Oral Mucosa and Palate Signs
Xerostomia, Sjögren syndrome. See Sjögren Syndrome, page 241 and Xerostomia page 234.
Buccal pigmentation—Addison disease. Small patches of pigment in the
buccal mucosa are common in blacks and other darkly pigmented races. In
whites, however, dappled brown pigment in the cheek’s lining strongly suggests Addison disease or Peutz–Jeghers syndrome.
Retention cyst. An obstructed mucous gland produces a blue-domed translucent cyst anywhere on the buccal surface.
Mucosal sebaceous cysts (Fordyce spots). The lip, cheek, and tongue mucosa
show isolated white or yellow, sometimes slightly raised, spots <1 mm in
diameter. Often a bit of white sebum may be expressed from the lesion. They
are painless and harmless.
Koplik spots (measles). Koplik spots are the earliest diagnostic sign of measles
and they are pathognomonic. One or two days before the exanthem appears,
small white spots appear opposite the molars, and sometimes elsewhere, on
the buccal mucosa (Fig. 7-60B). Each is surrounded by a narrow red areola.
Lichen planus. The lesions are thin, bluish-white, spiderweb lines resembling leukoplakia. Circumscribed areas of attened papules on the exor surfaces of the wrists and the mid shins support the diagnosis of lichen planus
(Chapter 6, page 138).
Leukoplakia. These precancerous lesions occur at sites of chronic irritation
from ill-tting dentures or smokeless tobacco. Tobacco and alcohol are cocarcinogens. The rst lesion is a whitened hyperkeratotic plaque. On the tongue,
one or more areas on the dorsal surface show obliteration of the papillae with
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FIG. 7- 60 Some Les ions of the Ora l Cavity. A. Subl ingual de rmoid cyst. B. Kopl ik spots. C. Torus p alatin us.
thin white lesions that are wrinkled and sometimes pearly. Persistent lesions
coalesce and enlarge, becoming chalk white, thickening and becoming more
rm than adjacent mucosa. Biopsy is indicated.
Thrush, candidiasis.
are diabetic, immunosuppressed (e.g.,
inhaled corticosteroids or have received broad spectrum antibiotics. The
lesions may be painless or cause mouth soreness, and the white plaques are
easily removed with a tongue blade. Less commonly, the mucosa is erythematous and thin, without the white plaques. Pain with swallowing suggests concomitant Candida esophagitis.
Telangiectasias—hereditary hemorrhagic telangiectasia. Early and obvious
lesions occur on the buccal mucosa, tongue, and lips. See Chapter 6, page 116.
Oral vesicles, blisters, and ulcers. Several diseases cause oral vesicles or
bullae, often with multiple ulcerations. The major disease mechanisms are
infection and immune-mediated processes. Larger ulcers are caused by tissue
destruction from infection, neoplasm, or metabolic causes.
Herpes simplex. Primary herpes simplex infection causes severe stomatitis
with painful vesicles that rupture forming shallow ulcers which heal slowly.
Herpangina. Coxsackievirus 16 infection results in fever and sore throat.
Exam shows small vesicles or whitish papules on the soft palate.
Lichen planus. Painful chronic ulcers may be surrounded by characteristic
lacy white mucosal lines.
Disseminated histoplasmosis. A persistent oral ulcer can be the presenting
sign of disseminated histoplasmosis. Diagnosis is made by biopsy.
Cicatricial pemphigoid.
al layer of the mucosa and skin lead to separation of the epithelial layers with
Oral infection with Candida spp. occurs in patients who
HIV, immunosuppressant drugs),
Autoantibodies against hemidesmosomes in the bas-
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blister formation. Pain is mild to moderate. The incidence increases with age.
Oral lesions may be accompanied by skin lesions (Chapter 6, page 147). The
course is chronic and recurrent. It must be distinguished from pemphigus
vulgaris (Chapter 6, page 146).
Stevens–Johnson syndrome. This is a severe allergic reaction with generalized involvement of the skin and mucous membranes. The most common cause is medication exposure. Early recognition, withdrawal of the
offending agent, and supportive therapy may be lifesaving.
Aphthous ulcer (canker sore). A few small vesicles appear in crops on the tip
and sides of the tongue and on the labial and buccal mucosa. After the vesicle
has ruptured, the lesion is a small, round, painful ulcer with a white oor,
yellow margins, and narrow surrounding erythematous areola. The cause is
unknown. Recurrent or persistent aphthous ulcers are seen in Crohn disease
and Behçet syndrome.
Mucous patches (condyloma latum). This is the common lesion of secondary
syphilis, occurring on the tongue and buccal and labial mucosae regardless of
the site of the primary lesion. The patches are round or oval, 5–10 mm in diameter, slightly raised, and covered by gray membrane. They may ulcerate slightly.
They feel indurated and are painless. Regional lymphadenopathy is common.
Osteonecrosis.
Ionizing irradiation, especially of the mandible, suppresses
normal bone turnover leading to acute or delayed bone necrosis with ulcerated overlying mucosa. Bisphosphonate therapy (especially intravenous
bisphosphonates for malignant hypercalcemia and myeloma) also suppresses
bone turnover and is associated with bone necrosis and mucosal ulceration.
Patients present with one or more slowly progressive often painful ulcerations
exposing underlying bone. A history of irradiation or bisphosphonate use is
essential for making the diagnosis. Formerly, exposures to white phosphorus
in the munitions industry caused a similar syndrome called phossy jaw.
Mucositis.
The bone marrow and oral and intestinal mucosae are the body’s
most rapidly proliferating tissues. Cytotoxic chemotherapy transiently stops
proliferation leading to impaired mucosal repair. Mouth ulcers occur 5–10
days after a cycle of cytotoxic chemotherapy. They may occur at any time
during chronic oral alkylating or antimetabolite therapy.
Reddened parotid duct orice—mumps. The parotid (Stensen) duct orice,
opposite the upper second molar, becomes reddened in mumps and other
acute parotitis.
Bony palate protuberance—torus. This common anatomic variation is a
bony knob or ridge in the midline of the hard palate. It is harmless.
Arched palate. There are many causes for high-arched palate. It is common in
Marfan and Turner syndromes.
Cleft palate. A midline opening in the hard palate results from congenital
failure of fusion of the maxillary processes. Usually associated with cleft lip,
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